| 武 曦,张 纲,冯晓丹,冯小倩,谭颖徽.缺氧通过HIF-1α抑制hPDLFs内毒素耐受[J].,2019,19(19):3611-3615 |
| 缺氧通过HIF-1α抑制hPDLFs内毒素耐受 |
| Hypoxia inhibits the Endotoxin Tolerance of hPDLFs by Upregulating HIF-1α Expression |
| 投稿时间：2019-02-23 修订日期：2019-03-18 |
| DOI：10.13241/j.cnki.pmb.2019.19.003 |
| 中文关键词: 牙周炎 牙周膜成纤维细胞 内毒素耐受 缺氧 缺氧诱导因子-1α |
| 英文关键词: Periodontitis hPDLFs Endotoxin tolerance Hypoxia HIF-1α |
| 基金项目:国家自然科学基金青年科学基金项目(81600873) |
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| 中文摘要: |
| 摘要 目的：观察缺氧对人牙周膜成纤维细胞(human Periodontal Ligament Fibroblasts，hPDLFs) 内毒素耐受(Endotoxin Tolerance，ET)的影响并初步探讨其可能作用机制。方法：人牙周膜经组织块和胰蛋白酶消化，原代分离培养hPDLFs并鉴定后，给予缺氧诱导，检测其炎症因子白介素-6(Interleukin 6，IL-6)和白介素-8(Interleukin 8，IL-8)的分泌情况。进一步在常氧环境下通过慢病毒过表达增强缺氧诱导因子-1α(Hypoxia Inducible Factor 1α, HIF-1α)表达或在缺氧环境下利用特异性抑制剂YC-1(3-(50-Hydroxymethyl-20-furyl)-1-benzylindazole)抑制hPDLFs中HIF-1α表达，分析hPDLFs炎症因子IL-6和IL-8的分泌情况的变化。结果：①缺氧时，脂多糖(Lipopolysaccharides，LPS)再次刺激hPDLFs分泌炎症因子白介素IL-6、IL-8没有明显减少(P>0.05)，提示hPDLFs的ET能力受到抑制。②常氧环境下，与HIF-1α未过表达组相比，过表达组的hPDLFs受到LPS再次刺激后，其分泌炎症因子IL-6或IL-8的能力并未显著降低(P>0.05)；而在缺氧环境下，hPDLFs HIF-1α表达受到抑制后，LPS再次刺激可以显著抑制hPDLFs分泌IL-6或IL-8(P<0.05)。结论：缺氧可能通过诱导HIF-1α抑制hPDLFs的ET，调节hPDLFs的免疫应答，从而加重牙周组织的免疫损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To observe the effect of hypoxia on the endotoxin tolerance (ET) of human periodontal ligament fibroblasts (hPDLFs), and preliminarily investigate the underlying mechanism. Methods: hPDLFs were cultured and identified after human periodontium were cut into pieces and digested with trypsin. Then to observe the effect of hypoxia and hypoxia inducible factor-1 alpha (HIF-1α) on the secretions of cytokines interleukin-6 (IL-6) and IL-8 by hPDLFs, HIF-1α was overexpressed by lentivirus vector in normoxia or inhibited by specific inhibitor YC-1 in hypoxia. Results: ① When hPDLFs were stimulated by lipopolysaccharides (LPS) again, the secretions of cytokines interleukin-6 (IL-6) and IL-8 were not significantly reduced compared with the initial stimulation in hypoxia (P>0.05), indicating that the activities of ET in hPDLFs were inhibited in hypoxia. ②Compared with the HIF-1α unoverexpressed group, the secretion of inflammatory factor IL-6 or IL-8 by hPDLFs was not significantly decreased in the HIF-1α overexpressed group upon LPS re-stimulation in normoxia (P>0.05), while the secretion was significantly inhibited when the expression of HIF-1α in hPDLFs was inhibited in hypoxia (P<0.05). Conclusion: Hypoxia may inhibit hPDLFs ET through inducing the expression of HIF-1α to enhance the immune injury of periodontal tissues, suggesting a new potential mechanism for hypoxia aggravating periodontitis. |
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